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Biological Effects of Targeted Gene Inactivation and Gene Transfer of the Coagulation and Fibrinolytic Systems in Mice

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Textbook of Coronary Thrombosis and Thrombolysis

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 193))

Abstract

Preservation of vascular integrity following traumatic or infectious challenges is essential for the survival of multicellular organisms. A major defense mechanism involves the formation of hemostatic plugs by activation of platelets and polymerization of fibrin. Initiation of the plasma coagulation system on exposure of blood to nonvascular cells is triggered by tissue factor (TF), which is expressed by a variety of cells surrounding the vasculature as a hemostatic envelope and which functions as a cellular receptor and cofactor for activation of the serine proteinase factor VII to VIIa [1]. This complex activates factor X directly or indirectly via activation of factor IX, resulting in the generation of thrombin-mediated conversion of fibrinogen to fibrin [2,3]. Thrombin and factor Xa produce a positive feedback stimulation of coagulation by activating factors VIII and V, which serve as membrane-bound receptors/cofactors for the proteolytic enzymes factors IXa and Xa, respectively [2,3].

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Carmeliet, P., Collen, D. (1997). Biological Effects of Targeted Gene Inactivation and Gene Transfer of the Coagulation and Fibrinolytic Systems in Mice. In: Becker, R.C. (eds) Textbook of Coronary Thrombosis and Thrombolysis. Developments in Cardiovascular Medicine, vol 193. Springer, Boston, MA. https://doi.org/10.1007/978-0-585-33754-8_6

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